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  1. Article ; Online: The Role of p53 in Metabolic Regulation.

    Puzio-Kuter, Anna M

    Genes & cancer

    2011  Volume 2, Issue 4, Page(s) 385–391

    Abstract: The metabolic changes that occur in a cancer cell have been studied for a few decades, but our appreciation of the complexity and importance of those changes is now being realized. The metabolic switch from oxidative phosphorylation to aerobic glycolysis ...

    Abstract The metabolic changes that occur in a cancer cell have been studied for a few decades, but our appreciation of the complexity and importance of those changes is now being realized. The metabolic switch from oxidative phosphorylation to aerobic glycolysis provides intermediates for cell growth and division and is regulated by both oncogenes and tumor suppressor genes. The p53 tumor suppressor gene has long been shown to play key roles in responding to DNA damage, hypoxia, and oncogenic activation. However, now p53 has added the ability to mediate metabolic changes in cells through the regulation of energy metabolism and oxidative stress to its repertoire of activities. It is therefore the focus of this review to discuss the metabolic pathways regulated by p53 and their cooperation in controlling cancer cell metabolism.
    Language English
    Publishing date 2011-07-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2538519-7
    ISSN 1947-6027 ; 1947-6019
    ISSN (online) 1947-6027
    ISSN 1947-6019
    DOI 10.1177/1947601911409738
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Correction: ARF Confers a Context-Dependent Response to Chemotherapy in Muscle-Invasive Bladder Cancer.

    Owczarek, Tomasz B / Kobayashi, Takashi / Ramirez, Ricardo / Rong, Lijie / Puzio-Kuter, Anna M / Iyer, Gopa / Teo, Min Yuen / Sánchez-Vega, Francisco / Wang, Jingqiang / Schultz, Nikolaus / Zheng, Tian / Solit, David B / Al-Ahmadie, Hikmat A / Abate-Shen, Cory

    Cancer research

    2023  Volume 83, Issue 7, Page(s) 1159

    Language English
    Publishing date 2023-04-04
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-23-0518
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The Role of the p53 Protein in Stem-Cell Biology and Epigenetic Regulation.

    Levine, Arnold J / Puzio-Kuter, Anna M / Chan, Chang S / Hainaut, Pierre

    Cold Spring Harbor perspectives in medicine

    2016  Volume 6, Issue 9

    Abstract: The p53 protein plays a passive and an active role in stem cells. The transcriptional activities of p53 for cell-cycle arrest and DNA repair are largely turned off in stem cells, but there is some indication that long-term stem-cell viability may require ...

    Abstract The p53 protein plays a passive and an active role in stem cells. The transcriptional activities of p53 for cell-cycle arrest and DNA repair are largely turned off in stem cells, but there is some indication that long-term stem-cell viability may require other p53-regulated functions. When p53 is activated in stem cells, it stops cell division and promotes the commitment to a differentiation pathway and the formation of progenitor cells. In the absence of any p53 activity, stem-cell replication continues and mistakes in the normal epigenetic pathway occur at a higher probability. In the presence of a functionally active p53 protein, epigenetic stability is enforced and stem-cell replication is regulated by commitment to differentiation. Over a lifetime of an organism, stem-cell clones compete in a tissue niche for Darwinian replicative advantages and in doing so accumulate mutations that permit stem-cell replication. Mutations in the p53 gene give stem cells this advantage, increase the clonal stem-cell population, and lower the age at which cancers can occur. Li-Fraumeni patients that inherit p53 mutations develop tumors in a tissue-type-specific fashion at younger ages. Throughout the life of a Li-Fraumeni patient, the tumor types that arise occur in tissues where stem cells are active and cell division is most rapid. Thus, p53 mutations that are inherited or occur during developmental life act in stem cells of the mesenchymal and epithelial lineages, whereas p53 mutations that occur in progenitor or differentiated (somatic) cells later in life function in tissues of endodermal origins, indicating that p53 may function differently in different developmental lineages.
    MeSH term(s) Cell Division ; DNA Replication ; Epigenesis, Genetic ; Humans ; Mutation ; Neoplasms/genetics ; Neoplasms/physiopathology ; Stem Cells/cytology ; Tumor Suppressor Protein p53/physiology
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2016-09-01
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2157-1422
    ISSN (online) 2157-1422
    DOI 10.1101/cshperspect.a026153
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The control of the metabolic switch in cancers by oncogenes and tumor suppressor genes.

    Levine, Arnold J / Puzio-Kuter, Anna M

    Science (New York, N.Y.)

    2010  Volume 330, Issue 6009, Page(s) 1340–1344

    Abstract: Cells from some tumors use an altered metabolic pattern compared with that of normal differentiated adult cells in the body. Tumor cells take up much more glucose and mainly process it through aerobic glycolysis, producing large quantities of secreted ... ...

    Abstract Cells from some tumors use an altered metabolic pattern compared with that of normal differentiated adult cells in the body. Tumor cells take up much more glucose and mainly process it through aerobic glycolysis, producing large quantities of secreted lactate with a lower use of oxidative phosphorylation that would generate more adenosine triphosphate (ATP), water, and carbon dioxide. This is the Warburg effect, which provides substrates for cell growth and division and free energy (ATP) from enhanced glucose use. This metabolic switch places the emphasis on producing intermediates for cell growth and division, and it is regulated by both oncogenes and tumor suppressor genes in a number of key cancer-producing pathways. Blocking these metabolic pathways or restoring these altered pathways could lead to a new approach in cancer treatments.
    MeSH term(s) Adenosine Triphosphate/metabolism ; Cell Division ; Citric Acid Cycle ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Glucose/metabolism ; Glutamine/metabolism ; Glycolysis ; Humans ; NADP/metabolism ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Oncogenes ; Pentose Phosphate Pathway ; Signal Transduction
    Chemical Substances Glutamine (0RH81L854J) ; NADP (53-59-8) ; Adenosine Triphosphate (8L70Q75FXE) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2010-12-03
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1193494
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  5. Article ; Online: The interfaces between signal transduction pathways: IGF-1/mTor, p53 and the Parkinson Disease pathway.

    Levine, Arnold J / Harris, Chris R / Puzio-Kuter, Anna M

    Oncotarget

    2012  Volume 3, Issue 11, Page(s) 1301–1307

    MeSH term(s) Animals ; Humans ; Insulin-Like Growth Factor I/metabolism ; Mice ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Tumor Suppressor Protein p53 ; Insulin-Like Growth Factor I (67763-96-6) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1)
    Language English
    Publishing date 2012-12-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.759
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Stem cell biology meets p53.

    Puzio-Kuter, Anna M / Levine, Arnold J

    Nature biotechnology

    2009  Volume 27, Issue 10, Page(s) 914–915

    MeSH term(s) Animals ; Cell Differentiation/physiology ; Cells, Cultured ; Fibroblasts/cytology ; Fibroblasts/metabolism ; Humans ; Mice ; Pluripotent Stem Cells/cytology ; Pluripotent Stem Cells/metabolism ; Stem Cells/cytology ; Stem Cells/metabolism ; Tumor Suppressor Protein p53/metabolism ; Xenopus laevis
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2009-10-08
    Publishing country United States
    Document type News
    ZDB-ID 1311932-1
    ISSN 1546-1696 ; 1087-0156
    ISSN (online) 1546-1696
    ISSN 1087-0156
    DOI 10.1038/nbt1009-914
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: DTIE, a novel core promoter element that directs start site selection in TATA-less genes.

    Marbach-Bar, Nadav / Bahat, Anat / Ashkenazi, Shaked / Golan-Mashiach, Michal / Haimov, Ora / Wu, Shwu-Yuan / Chiang, Cheng-Ming / Puzio-Kuter, Anna / Hirshfield, Kim M / Levine, Arnold J / Dikstein, Rivka

    Nucleic acids research

    2016  Volume 44, Issue 3, Page(s) 1080–1094

    Abstract: The transcription start site (TSS) determines the length and composition of the 5' UTR and therefore can have a profound effect on translation. Yet, little is known about the mechanism underlying start site selection, particularly from promoters lacking ... ...

    Abstract The transcription start site (TSS) determines the length and composition of the 5' UTR and therefore can have a profound effect on translation. Yet, little is known about the mechanism underlying start site selection, particularly from promoters lacking conventional core elements such as TATA-box and Initiator. Here we report a novel mechanism of start site selection in the TATA- and Initiator-less promoter of miR-22, through a strictly localized downstream element termed DTIE and an upstream distal element. Changing the distance between them reduced promoter strength, altered TSS selection and diminished Pol II recruitment. Biochemical assays suggest that DTIE does not serve as a docking site for TFIID, the major core promoter-binding factor. TFIID is recruited to the promoter through DTIE but is dispensable for TSS selection. We determined DTIE consensus and found it to be remarkably prevalent, present at the same TSS downstream location in ≈20.8% of human promoters, the vast majority of which are TATA-less. Analysis of DTIE in the tumor suppressor p53 confirmed a similar function. Our findings reveal a novel mechanism of transcription initiation from TATA-less promoters.
    MeSH term(s) Animals ; Base Sequence ; HEK293 Cells ; Humans ; MicroRNAs/genetics ; Promoter Regions, Genetic ; Sequence Homology, Nucleic Acid ; TATA Box/genetics ; Transcription, Genetic
    Chemical Substances MIRN22 microRNA, human ; MicroRNAs
    Language English
    Publishing date 2016-02-18
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkv1032
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    Zs.A 1067: Show issues Location:
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  8. Article: The Control of the Metabolic Switch in Cancers by Oncogenes and Tumor Suppressor Genes

    Levine, Arnold J / Puzio-Kuter, Anna M

    Science. 2010 Dec. 3, v. 330, no. 6009

    2010  

    Abstract: Cells from some tumors use an altered metabolic pattern compared with that of normal differentiated adult cells in the body. Tumor cells take up much more glucose and mainly process it through aerobic glycolysis, producing large quantities of secreted ... ...

    Abstract Cells from some tumors use an altered metabolic pattern compared with that of normal differentiated adult cells in the body. Tumor cells take up much more glucose and mainly process it through aerobic glycolysis, producing large quantities of secreted lactate with a lower use of oxidative phosphorylation that would generate more adenosine triphosphate (ATP), water, and carbon dioxide. This is the Warburg effect, which provides substrates for cell growth and division and free energy (ATP) from enhanced glucose use. This metabolic switch places the emphasis on producing intermediates for cell growth and division, and it is regulated by both oncogenes and tumor suppressor genes in a number of key cancer-producing pathways. Blocking these metabolic pathways or restoring these altered pathways could lead to a new approach in cancer treatments.
    Keywords adenosine triphosphate ; adults ; carbon dioxide ; cell growth ; Gibbs free energy ; glucose ; glycolysis ; lactic acid ; neoplasm cells ; neoplasms ; oncogenes ; oxidative phosphorylation ; tumor suppressor genes
    Language English
    Dates of publication 2010-1203
    Size p. 1340-1344.
    Publishing place American Association for the Advancement of Science
    Document type Article
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1193494
    Database NAL-Catalogue (AGRICOLA)

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  9. Article ; Online: ARF Confers a Context-Dependent Response to Chemotherapy in Muscle-Invasive Bladder Cancer.

    Owczarek, Tomasz B / Kobayashi, Takashi / Ramirez, Ricardo / Rong, Lijie / Puzio-Kuter, Anna M / Iyer, Gopa / Teo, Min Yuen / Sánchez-Vega, Francisco / Wang, Jingqiang / Schultz, Nikolaus / Zheng, Tian / Solit, David B / Al-Ahmadie, Hikmat A / Abate-Shen, Cory

    Cancer research

    2017  Volume 77, Issue 4, Page(s) 1035–1046

    Abstract: Muscle-invasive bladder cancer (MIBC) generally responds poorly to treatment and tends to exhibit significant mortality. Here we show that expression of the tumor suppressor ... ...

    Abstract Muscle-invasive bladder cancer (MIBC) generally responds poorly to treatment and tends to exhibit significant mortality. Here we show that expression of the tumor suppressor p14
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Animals ; Cell Line, Tumor ; Cisplatin/therapeutic use ; DNA Damage ; Drug Resistance, Neoplasm ; Female ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Neoplasm Invasiveness ; Nuclear Proteins/physiology ; Tumor Suppressor Protein p14ARF/analysis ; Tumor Suppressor Protein p14ARF/physiology ; Tumor Suppressor Protein p53/physiology ; Urinary Bladder Neoplasms/drug therapy ; Urinary Bladder Neoplasms/pathology ; Xenograft Model Antitumor Assays
    Chemical Substances ITGB3BP protein, human ; Nuclear Proteins ; Tumor Suppressor Protein p14ARF ; Tumor Suppressor Protein p53 ; Cisplatin (Q20Q21Q62J)
    Language English
    Publishing date 2017-01-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-16-2621
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  10. Article ; Online: Mouse models of human bladder cancer as a tool for drug discovery.

    Seager, Catherine / Puzio-Kuter, Anna M / Cordon-Cardo, Carlos / McKiernan, James / Abate-Shen, Cory

    Current protocols in pharmacology

    2010  Volume Chapter 14, Page(s) Unit14.14

    Abstract: Muscle-invasive bladder cancer is a deadly condition in dire need of effective new treatments. This unit contains a description of mouse models suitable for the evaluation of potential new therapies. Included is a genetically engineered mouse model of ... ...

    Abstract Muscle-invasive bladder cancer is a deadly condition in dire need of effective new treatments. This unit contains a description of mouse models suitable for the evaluation of potential new therapies. Included is a genetically engineered mouse model of bladder cancer generated by the delivery of an adenovirus expressing Cre recombinase into the bladder lumen. Also described is an orthotopic mouse model created by the instillation of human bladder tumor cells into the bladder lumen of immune deficient mice. Protocols are also provided on the use of these models for the preclinical evaluation of new chemical entities, with mTOR inhibitors shown as an example.
    MeSH term(s) Adenoviridae ; Animals ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Disease Models, Animal ; Drug Discovery/methods ; Female ; Genetic Engineering/methods ; Genetic Vectors ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Specimen Handling/methods ; Urinary Bladder Neoplasms/drug therapy
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2010-04-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2179074-7
    ISSN 1934-8290 ; 1934-8282
    ISSN (online) 1934-8290
    ISSN 1934-8282
    DOI 10.1002/0471141755.ph1414s49
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